Day: 20150920

Summary:The brains of endurance trainers communicate with muscles differently than those of strength trainers or sedentary individuals, new research shows. While it is not immediately clear why the communication between the brain and muscle was different as a result of different types of exercise, one researcher said it offers leads for new means of research into neuromechanical differences in muscle function, muscle performance, muscle stiffness and other areas.

A University of Kansas study shows that the communication between the brain and quadriceps muscles of people who take part in endurance training, such as running long distances, is different than those who regularly took part in resistance training and those who were sedentary. The findings may offer clues to the type of physical activity humans are most naturally suited to.

Trent Herda, assistant professor of health, sport and exercise sciences, and Michael Trevino, a doctoral student, conducted studies in which they measured muscle responses of five people who regularly run long distances, five who regularly lift weights and five sedentary individuals who regularly do neither. The studies have been published in the Journal of Sports Sciences and Muscle and Nerve.

Among the findings, Herda and Trevino showed that the quadriceps muscle fibers of the endurance trainers were able to fire more rapidly.

“The communication between the brains and their muscles was slightly different than the resistance trainers and sedentary individuals,” Herda said of endurance trainers. “This information also suggested that resistance trainers and those who are sedentary were more likely to fatigue sooner, among other things.”

Survey participants were 15 healthy volunteers. The endurance trainers had consistently taken part in a structured running program for at least three years prior to the study and ran an average of 61 miles a week and did not take part in resistance training. The resistance trainers had consistently taken part in a weight-training program for at least four years prior to the study. They took part in resistance training four to eight hours per week and reported doing at least one repetition of a back squat of twice their body mass. One reported doing a squat of 1.5 times his or her body weight, but none engaged in aerobic activity such as swimming, jogging or cycling. The sedentary participants did not take part in any structured physical exercise for three years prior to the study.

Participants wore mechanomyographic and electromyographic electrode sensors on their quadriceps muscle and extended their leg while seated. The researchers measured submaximal contraction and total force by having participants extend their leg, then exert more force, attempting to achieve from 40 to 70 percent of total force, which they could see represented in real time on a computer screen.

While it is not immediately clear why the communication between the brain and muscle was different as a result of different types of exercise as evidenced by the difference in rates of muscle fibers firing, Herda said it offers leads for new means of research into neuromechanical differences in muscle function, muscle performance, muscle stiffness and other areas. It also provides several clues into the type of exercise humans are more naturally built for. While not claiming that one type of exercise or sport is superior to another, Herda said the findings suggest that the human body’s neuromuscular system may be more naturally inclined to adapt to aerobic exercise than resistance training for strength as the communication between the brain and muscles was similar between resistance training and sedentary individuals.

Summary:Cellular interactions that trigger the production of myelin are especially hard to pinpoint. That’s because the crucial point of contact between two types of cells — the connection between axons, along which nerve impulses travel, and glial cells, which support neurons — is essentially hidden. Now, in a new article, researchers explain a new method to more precisely capture how brain cells interact.

Now, University at Buffalo researchers and their colleagues at other institutions are publishing a paper online in Nature Communications on Sept. 18 about a new method they developed to more precisely capture how brain cells interact.

The work was led by scientists at UB’s Hunter James Kelly Research Institute (HJKRI) who conduct research to better understand myelin, the fatty insulator that enables communication between nerve cells. The researchers study how damage to myelin occurs, and how that damage may be repaired. The institute, part of UB’s New York State Center of Excellence in Bioinformatics and Life Sciences, was established in 1997 by Buffalo Bills Hall of Fame quarterback Jim Kelly and his wife Jill after their infant son Hunter, was diagnosed with Krabbe Leukodystrophy, an inherited fatal disorder. He died in 2005 at the age of 8.

The researchers explained that cellular interactions that trigger the production of myelin are especially hard to pinpoint. That’s because the crucial point of contact between two types of cells — the connection between axons, along which nerve impulses travel, and glial cells, which support neurons — is essentially hidden.

“Myelin is made by a glial cell wrapping around an axon cell,” explained M. Laura Feltri, MD, senior author on the paper and an HJKRI researcher and professor of biochemistry and neurology in the Jacobs School of Medicine and Biomedical Sciences at UB. “To study myelin, you really need to study both cells. The glial cell wraps like a spiral around the axon, so every time you try to study the region of contact between the two cells, you end up studying the whole combination. It’s very hard to look just at the interface.”

And studying this interface is critical in certain diseases, she added.

“In Krabbe’s, for example, the problem is not just that there isn’t sufficient myelin, but that the glial cell is not providing proper support to the neuron. But to figure out exactly what’s going wrong, we needed a better way to study that interface.” The new technique for achieving this involves using the second cell (the neuron) as a trigger to attract the first cell (the glial cell). The researchers use a system with two chambers, separated by a membrane.

“When the cells in the upper chamber ‘recognize’ the cells in the bottom chamber, they kind of ‘reach’ through the holes in the membrane for each other and touch. That is the intersection that we can then isolate and study,” Feltri explained.

Using this technique, the researchers discovered novel proteins at that intersection called prohibitins, which, they found, are necessary for the production of myelin. The discovery will help improve the understanding of and development of new treatments for myelin diseases. It also will make it easier to study all kinds of cellular interactions, not just those in the brain.

“Using this method, we can isolate the portion of a cell that comes in contact with another cell, and analyze all the proteins that are present only in this subcellular fraction,” Feltri explained. “It’s provides a glimpse into the social life of cells.” “This work has important implications for diseases of myelin such as Krabbe disease, and other neurodegenerative diseases, because the communication between glial cells and neurons is vital for neuroprotection,” she said.

Yannick Poitelon, PhD, postdoctoral research scientist at HJKRI and first author of the paper, explained that glial cells support neurons metabolically and protect axons that can measure up to one meter in length, extending far away from the glial cell.

“This has profound implications for glial disease like Krabbe’s, Charcot-Marie Tooth, peripheral neuropathies or Multiple Sclerosis, because the dysfunction of glial cells end up impairing the interactions with neurons, which as a result suffer and degenerate causing devastating clinical symptoms,” said Poitelon. “Similarly, neurodegenerative diseases like Huntington’s disease or Lou Gehrig’s, that were considered uniquely diseases of neurons in the past, are now considered diseases of cellular communications between neurons and glial cells.”

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The above post is reprinted from materials provided by University at Buffalo. The original item was written by Ellen Goldbaum. Note: Materials may be edited for content and length.